Filter by keywords:



Filtering documents. Please wait...

11/37. codeine phosphate-induced hypersensitivity syndrome.

    OBJECTIVE: To report a case of drug-induced hypersensitivity syndrome related to codeine phosphate. CASE SUMMARY: A 19-year-old Japanese man was prescribed codeine phosphate 10 mg 3 times daily and several other drugs for cold symptoms. About 20 days later, an erythematous, maculopapular rash appeared and progressed to erythroderma; a spiking fever also developed. He had splenomegaly and generalized lymphadenopathy on admission. Laboratory examinations showed atypical lymphocytosis, eosinophilia, and increased liver enzyme values. The platelet count slowly decreased after admission. The increased numbers of megakaryocytes in bone marrow and platelet-associated immunoglobulin (Ig) G antibodies in serum were compatible with a diagnosis of immune thrombocytopenic purpura. A significant increase in IgG antibodies to human herpesvirus 6 (HHV6) and transient viremia were helpful in diagnosing hypersensitivity syndrome. The results of patch tests were positive for codeine phosphate. An objective causality assessment revealed that an adverse drug event was probable. DISCUSSION: codeine is an opioid analgesic. Severe adverse cutaneous reactions rarely occur. As of March 3, 2004, our case is, to our knowledge, the first report of hypersensitivity syndrome attributed to codeine phosphate. Drug-induced hypersensitivity syndrome is an acute, potentially life-threatening, idiosyncratic adverse reaction caused mainly by aromatic anticonvulsants. It is characterized by the triad of fever, skin rash, and internal organ involvement. Reactivation of HHV6 is involved in the pathogenesis of this syndrome and may have also caused the immune thrombocytopenic purpura in our patient. CONCLUSIONS: codeine phosphate may rarely be associated with hypersensitivity syndrome. Clinicians should be aware that the potentially fatal syndrome can be caused by various drugs.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

12/37. A case of 'auto-immune thrombocytopenic purpura' serologically similar to post-transfusion purpura.

    The report describes a HPA-1a (Zwa)-negative woman with thrombocytopenia and antibodies in serum and eluate from autologous platelets with an operational anti-HPA-1a specificity. The results of the serological investigations were similar to the findings in most patients suffering from post-transfusion purpura. However, the present patient had no history of blood transfusion prior to the unset of purpura and the thrombocytopenia had persisted 6 months before splenectomy.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

13/37. Development of Perthes' disease in a 3-year-old boy with idiopathic thrombocytopenic purpura and antiphospholipid antibodies.

    A 3-year-old boy developed idiopathic thrombocytopenic purpura (ITP) and Perthes' disease concurrently. Antiphospholipid antibodies were detected in the serum of the patient. Therefore, it is possible that Perthes' disease in this patient might be one of the manifestations of ITP-associated antiphospholipid syndrome.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

14/37. Relevance of the HPA-15 (Gov) polymorphism on CD109 in alloimmune thrombocytopenic syndromes.

    BACKGROUND: Alloantibodies against the human platelet (PLT) alloantigen (HPA)-15 system residing on CD109 can cause fetal and neonatal alloimmune thrombocytopenia (FNAIT), posttransfusion purpura, and PLT transfusion refractoriness. The detection of antibodies against HPA-15, however, is hampered by the variable low expression and instability of the CD109 molecule during preparation and storage. STUDY DESIGN AND methods: This study analyzed the occurrence of HPA-15 alloantibodies in 1403 patients: 930 FNAIT and 473 polytransfused (PT) patients by modified monoclonal antibody specific immobilization of PLT antigens (MAIPA) assay with well-defined phenotyped PLTs. A dna typing technique was developed to confirm the phenotypes of PLT donors. B-cell lines were established as sources of reference dna. RESULTS: Genotyping of 407 unrelated blood donors revealed the gene frequencies 0.512 and 0.488 for HPA-15a and -15b, respectively. Based on the selection of PLTs expressing high amounts of CD109 on the surface (mean fluorescence intensity ratio 4-5 on expression peak on Days 2-4 after apheresis) antibody screening by the MAIPA assay was performed. In total, 16 (1.1%) HPA-15 alloantibodies were found comprising four anti-HPA-15a and 12 anti-HPA-15b. Anti-HPA-15b without other PLT-reactive antibodies were detectable in three serum samples of PT patients. The incidence of HPA-15 alloimmunization in PT patients was significantly higher than in mothers with FNAIT (3.0% vs. 0.22%). In relation to all detected HPA-specific antibodies, HPA-15 is responsible for 6.2 percent of alloimmunizations. CONCLUSION: These observations indicate that alloimmunization against HPA-15 should be considered as a cause for immune thrombocytopenia, particularly in patients receiving multiple PLT transfusions.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

15/37. Anti-HPA-1a in a case of post-transfusion purpura: binding to antigen-negative platelets detected by adsorption/elution.

    Post-transfusion purpura (PTP) is a rare transfusion reaction almost exclusively observed in female patients. Affected patients develop severe immune-mediated thrombocytopenia in the course of a strong anamnestic alloimmune reaction against a platelet-specific antigen. The pathophysiology of thrombocytopenia has remained elusive. Immunological analysis in the HPA-1a-alloimmunized patient described in this report revealed an antibody with features considered typical of PTP: not only was anti-HPA-1a detectable in plasma, but it could also be eluted from the patients' (alloantigen negative) platelets, and anti-HPA-1a could be detected in eluates from both antigen positive and negative test platelets, which had been incubated in the patient's serum. This is in contrast to two sera with HPA-1a alloantibodies obtained from mothers of children with neonatal alloimmmune thrombocytopenia which were strictly HPA-1a specific. It is proposed that alloantibodies with HPA-1a-like specificity explain the patient's immune thrombocytopenia. The technique described in this report is proposed for further investigation, as it might be useful for discrimination of alloantibodes in PTP and alloantibodies of transfused thrombocytopenic patients.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

16/37. Severe thrombocytopenia due to host-derived anti-HPA-1a after non-myeloablative allogeneic haematopoietic stem cell transplantation for multiple myeloma: a case report.

    BACKGROUND AND OBJECTIVES: Host- or donor-derived alloimmune thrombocytopenia can develop after non-myeloablative allogeneic haematopoietic stem cell transplantation (HSCT). We report the first case of host-derived HPA-1a antibodies. CASE REPORT: A 52-year-old male patient received HSCT from his human leucocyte antigen (HLA)-A, -B, -C, -DR identical brother after reduced intensity conditioning. Bilinear engraftment around day 12 was accompanied by a continuous decrease of platelet counts. We investigated for platelet antibodies because of a progressive decline of platelet counts and refractoriness to platelet transfusions. methods: The patient's serum was tested by enzyme-linked immunosorbent assay (ELISA), a solid phase assay and monoclonal antibody-specific immobilization of platelet antigens (MAIPA) assay. Recipient's dna from the time before HSCT and donor's dna were genotyped for human platelet antigens. RESULTS: serum obtained on day 15 after HSCT reacted strongly with the donor's platelets due to host-derived anti-HPA-1a- and anti-HLA I antibodies. serum samples from days 39, 45 and 65 after HSCT contained only anti-HLA I; no antibodies were detectable on day 149. Platelet counts increased on day 20 spontaneously. The decrease of the antibodies accompanied by the increase of the platelet counts suggests progressive elimination of residual host cells. CONCLUSIONS: The HPA-1a antibodies affected thrombopoietic engraftment and the success of platelet transfusions.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

17/37. Rosiglitazone-induced immune thrombocytopenia.

    Rosiglitazone is one of the members in the thiazolidinedione (TZD) class of anti-diabetic agents that have proven efficacy in the treatment of patients with type 2 diabetes. We studied serum from a patient who developed acute, severe thrombocytopenia after exposure to rosiglitazone maleate (Avandia) and proposed the mechanisms for rosiglitazone-induced thrombocytopenia. Tested by flow cytometry, the patient's serum was positive for rosiglitazone-induced antibody with the binding ratio of 5.93 (mean fluorescence intensity, MFI) in the presence of the patient's serum and rosiglitazone in a final concentration of 0.53 mmol/l. The antibody was found to bind both glycoprotein (GP) IIb-IIIa complex and GP Ib/IX complex by MAIPA assay using five different monoclonal antibodies (mAbs) against GP complexes Ib/IX, GPIIb/IIIa or GPIa/IIa. immunoprecipitation studies showed that both GPIIb/IIIa and GP Ib/IX complex were precipitated by antibody in the presence, but not in the absence of rosiglitazone. These findings provide evidence that immune thrombocytopenia can be caused by sensitivity to the antidiabetic agent rosiglitazone maleate. This report documents the first case of rosiglitazone-induced immune thrombocytopenia.
- - - - - - - - - -
ranking = 3
keywords = serum
(Clic here for more details about this article)

18/37. A pregnant woman with complications of lymphangioleiomyomatosis and idiopathic thrombocytopenic purpura.

    A pregnant 26-year-old woman developed hemosputum, dyspnea and pneumothorax. lymphangioleiomyomatosis was suspected based on multiple cystic lesions on chest computed tomography. Additionally, moderate thrombocytopenia occurred during the last trimester. hyperplasia of megakaryocytes in a bone marrow specimen and a high serum titer of platelet-associated IgG led to a diagnosis of idiopathic thrombocytopenic purpura. High-dose intravenous gammaglobulin promptly restored her platelet count, and the patient successfully gave birth to a healthy baby by cesarean section. After delivery, lymphangioleiomyomatosis was diagnosed by lung biopsy that was obtained during a video-assisted thoracoscopic abscission for recurrent pneumothorax. Underlying lymphangioleiomyomatosis and idiopathic thrombocytopenic purpura may be obviated by pregnancy.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

19/37. Cyclic thrombocytopenia associated with IgM anti-GPIIb-IIIa autoantibodies.

    We studied a female patient with cyclic fluctuation in platelet count following splenectomy for autoimmune thrombocytopenia. The cyclical fluctuation appeared to be in phase with her menstrual cycle and her platelet count was low during menses. bone marrow examinations performed at the peak as well as the bottom of the platelet count showed normal or increased numbers of megakaryocytes. The patient's platelet count increased rapidly after intravenous gamma-globulin (IVIgG) therapy, suggesting that a failure of platelet production is unlikely to account for the cycle. Platelet-associated IgM (PAIgM) was markedly elevated, whereas PAIgG was normal at any stage of the cycle. MACE assay demonstrated that PAIgM contained IgM anti-glycoprotein (GP) IIb-IIIa autoantibodies. Comparison between MACE assay using untreated and EDTA-treated platelets at 37 degrees C demonstrated that the platelet-associated IgM autoantibodies mainly recognized divalent cation-dependent conformation(s) of GPIIb-IIIa. No antibodies were, however, detected in her serum. The levels of IgM anti-GPIIb-IIIa showed an inverse relationship with the platelet count. In spite of the marked increase in platelet count after IVIgG, however, the levels of IgM anti-GPIIb-IIIa remained elevated. These findings suggest that platelet-associated IgM anti-GPIIb-IIIa autoantibodies are of pathogenic significance in this patient.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)

20/37. Selective iga deficiency with unusual features: development of common variable immunodeficiency, sjogren's syndrome, autoimmune hemolytic anemia and immune thrombocytopenic purpura.

    We report on a girl with selective iga deficiency and persistently low complement component 4 (C4) levels compatible with heterozygous C4 deficiency. Deterioration of her serum immunoglobulin levels and transition to common variable immunodeficiency were observed within a 5 year follow-up. She also developed sjogren's syndrome, autoimmune hemolytic anemia and immune thrombocytopenic purpura. While these abnormalities have been described before in various combinations, to our knowledge, they have not been reported in a single individual.
- - - - - - - - - -
ranking = 1
keywords = serum
(Clic here for more details about this article)
<- Previous || Next ->



We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.